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Titolo:
Increasing endothelial cell permeability improves the efficiency of myocyte adenoviral vector infection
Autore:
Nevo, N; Chossat, N; Gosgnach, W; Logeart, D; Mercadier, JJ; Michel, JB;
Indirizzi:
CHU Xavier Bichat, Fac Med, INSERM, U460, F-75018 Paris, France CHU XavierBichat Paris France F-75018 SERM, U460, F-75018 Paris, France
Titolo Testata:
JOURNAL OF GENE MEDICINE
fascicolo: 1, volume: 3, anno: 2001,
pagine: 42 - 50
SICI:
1099-498X(200101/02)3:1<42:IECPIT>2.0.ZU;2-2
Fonte:
ISI
Lingua:
ENG
Soggetto:
VIVO GENE-TRANSFER; IN-VIVO; REPLICATION-DEFICIENT; BARRIER FUNCTION; HEART; MONOLAYERS; THROMBIN; MACROMOLECULES; MYOCARDIUM; HISTAMINE;
Keywords:
endothelium; cardiac myocytes; adenoviral vector; permeability; thrombin; gene therapy;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Nevo, N CHU Xavier Bichat, Fac Med, INSERM, U460, 16 Rue Henri Huchard, F-75018 Paris, France CHU Xavier Bichat 16 Rue Henri Huchard Paris France F-75018 rance
Citazione:
N. Nevo et al., "Increasing endothelial cell permeability improves the efficiency of myocyte adenoviral vector infection", J GENE MED, 3(1), 2001, pp. 42-50

Abstract

Background Gene delivery to the myocardium using blood-borne adenoviral vectors is hindered by the endothelium, which represents a barrier limiting the infection rate of underlying myocytes. However, endothelial permeabilitymay be modulated by pharmacological agents. Methods In the present study, we modeled the endothelial barrier in vitro using a human umbilical vein endothelial cell (HUVEC) monolayer seeded on aTranswell membrane as a support and diffusion of fluorescent dextrans as apermeability index. We used alpha -thrombin (100 nM) as a pharmacological agent known to increase endothelial permeability and tested the barrier function of the endothelial cell monolayer on adenovector-mediated luciferase gene transfer to underlying isolated cardiac myocytes. Results A confluent HUVEC monolayer represented a considerable physical barrier to dextran diffusion; it reduced the permeability of the micropore membrane alone to fluorescein isothiocyanate (FITC)-labeled dextrans of molecular weights 4, 70, 150 and 2000 kDa by approximately 54, 78, 88 and 98%, respectively. alpha -Thrombin (100 nM) increased the permeability coefficients (P-EC) by 276, 264, 562 and 4166% for the same dextrans, respectively. Aconfluent HUVEC monolayer represented a major impediment to adenovector-mediated luciferase gene transfer to cardiac myocytes, largely reducing gene transfer efficiency. However thrombin induced a nine-fold increase in myocyte infection. Conclusion In our model, the endothelial cell monolayer represents a majorimpediment to myocyte adenovector-mediated gene transfer which can be partially improved by pharmacologically increasing endothelial permeability. The Transwell model is therefore particularly useful for testing the efficiency of pharmacological agents in modulating adenovector passage through the endothelial barrier. Copyright lj 2000 John Wiley & Sons, Ltd.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/01/20 alle ore 21:05:37